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Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation
The cytoplasmic domain of lentiviral Envelopes (EnvCD) ensures Env incorporation into nascent virions and regulates Env trafficking to and from the plasma membrane. It has also been reported to promote transcription from the viral LTR both directly and indirectly. Noticeably, the HIV-1 and SIV(mac23...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5816530/ https://www.ncbi.nlm.nih.gov/pubmed/29454367 http://dx.doi.org/10.1186/s12985-018-0941-7 |
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author | Beraud, Cyprien Lemaire, Morgane Perez Bercoff, Danielle |
author_facet | Beraud, Cyprien Lemaire, Morgane Perez Bercoff, Danielle |
author_sort | Beraud, Cyprien |
collection | PubMed |
description | The cytoplasmic domain of lentiviral Envelopes (EnvCD) ensures Env incorporation into nascent virions and regulates Env trafficking to and from the plasma membrane. It has also been reported to promote transcription from the viral LTR both directly and indirectly. Noticeably, the HIV-1 and SIV(mac239) EnvCDs were described to trigger nuclear translocation of NF-κB (Postler, Cell Host Microbes 2012). Given the paramount importance of identifying viral and host factors regulating HIV transcription, cellular signaling pathways and latency, and given that viral replication capacity is dependent on Env, we asked whether HIV EnvCDs from different HIV-1 subtypes differently modulated NF-κB. To that aim, we evaluated the ability of primary HIV-1 Envs from subtypes B and C to activate the NF-κB pathway. Primary subtype B and C Envs all failed to activate the NF-κB pathway. In contrast, when the EnvCD of HIV-1 Envs was fused to the the CD8-α chain, it induced ~ 10-fold increase in NF-κB induction, and this increase was much stronger with a truncated form of the HIV EnvCD lacking the 76 C-terminal residues and containing the proposed TAK-1 binding domain. Our results indicate that the HIV-1 EnvCD is unlikely to trigger the NF-κB pathway in its native trimeric form. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12985-018-0941-7) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5816530 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-58165302018-02-21 Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation Beraud, Cyprien Lemaire, Morgane Perez Bercoff, Danielle Virol J Short Report The cytoplasmic domain of lentiviral Envelopes (EnvCD) ensures Env incorporation into nascent virions and regulates Env trafficking to and from the plasma membrane. It has also been reported to promote transcription from the viral LTR both directly and indirectly. Noticeably, the HIV-1 and SIV(mac239) EnvCDs were described to trigger nuclear translocation of NF-κB (Postler, Cell Host Microbes 2012). Given the paramount importance of identifying viral and host factors regulating HIV transcription, cellular signaling pathways and latency, and given that viral replication capacity is dependent on Env, we asked whether HIV EnvCDs from different HIV-1 subtypes differently modulated NF-κB. To that aim, we evaluated the ability of primary HIV-1 Envs from subtypes B and C to activate the NF-κB pathway. Primary subtype B and C Envs all failed to activate the NF-κB pathway. In contrast, when the EnvCD of HIV-1 Envs was fused to the the CD8-α chain, it induced ~ 10-fold increase in NF-κB induction, and this increase was much stronger with a truncated form of the HIV EnvCD lacking the 76 C-terminal residues and containing the proposed TAK-1 binding domain. Our results indicate that the HIV-1 EnvCD is unlikely to trigger the NF-κB pathway in its native trimeric form. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12985-018-0941-7) contains supplementary material, which is available to authorized users. BioMed Central 2018-02-17 /pmc/articles/PMC5816530/ /pubmed/29454367 http://dx.doi.org/10.1186/s12985-018-0941-7 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Short Report Beraud, Cyprien Lemaire, Morgane Perez Bercoff, Danielle Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation |
title | Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation |
title_full | Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation |
title_fullStr | Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation |
title_full_unstemmed | Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation |
title_short | Reassessment of the capacity of the HIV-1 Env cytoplasmic domain to trigger NF-κB activation |
title_sort | reassessment of the capacity of the hiv-1 env cytoplasmic domain to trigger nf-κb activation |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5816530/ https://www.ncbi.nlm.nih.gov/pubmed/29454367 http://dx.doi.org/10.1186/s12985-018-0941-7 |
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